Mediated largely by a family of Toll-like-receptors (TLR) and associated intracellular downstream signaling molecules, the human innate immune response serves multiple functions ranging from providing the first line of defense to coordinating cellular growth as well as other cellular functions. Biochemical studies and genetic analyses using transgenic mice have revealed specific ligands for several TLR receptors. TLR have intracellular domains that can specifically recruit several adaptor proteins including MyD88, TIRAP/MAL, TRIF, and TOLLIP. These adaptor proteins subsequently associate with a family of interleukin-1 receptor-associated kinases (IRAK1, 2, M, and 4). Recruitments of numerous downstream signaling proteins leads to activation of a range of transcription factors such as NF kappa B, AP-1, and IRFs, which are responsible for specific gene transcriptions. Human innate immunity is manifested in diverse cells and tissues. Well-coordinated innate immunity signaling enables human cells and tissues to properly respond to various substances. Improper regulations of such events can lead to excessive signaling via TLRs, thus leading to inflammation. Such inflammation can involve more than one TLR. Therefore, there is a need in the art for new therapies that can modulate one or more TLR in order to reduce inflammation that occurs via multiple TLR pathways.